Lipoprotein-associated phospholipase A2

被引：48
作者：
McConnell, Joseph P.
Hoefner, Daniel M.
机构：
[1] Mayo Clin & Mayo Fdn, Dept Lab Med & Pathol, Rochester, MN 55905 USA
[2] Lab Corp Amer, Dept Sci & Technol, Elon, NC 27244 USA
来源：
CLINICS IN LABORATORY MEDICINE | 2006年 / 26卷 / 03期
关键词：
D O I：
10.1016/j.cll.2006.06.003
中图分类号：
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号：
1001 ;
摘要：
Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is an emerging inflammatory marker that is used to assess the risk for cardiovascular disease (CVD) and associated events. Several epidemiologic studies have demonstrated an independent association between plasma Lp-PLA2 concentration and risk for cardiovascular events. HMG-CoA reductase inhibitors (statins) and fenofibrates can reduce Lp-PLA2 concentrations in plasma, and orally active, specific Lp-PLA2 inhibitors have been developed and are in clinical trials to evaluate the potential of Lp-PLA2 as a therapeutic target. This article reviews recent studies of Lp-PLA2 in the setting of CVD, discusses the proposed mechanisms of action of Lp-PLA2, and describes methods for measurement and their clinical application. Recent evidence that suggests Lp-PLA(2)'S potential usefulness as a therapeutic target also is reviewed.
引用
收藏
页码：679 / +
页数：20
相关论文
共 56 条
[1]   The effect of statin therapy on lipoprotein associated phospholipase A2 levels [J].
Albert, MA ;
Glynn, RJ ;
Wolfert, RL ;
Ridker, PM .
ATHEROSCLEROSIS, 2005, 182 (01) :193-198
[2]   Lipoprotein-associated phospholipase A2, high-sensitivity C-reactive protein, and risk for incident ischemic stroke in middle-aged men and women in the Atherosclerosis Risk in Communities (ARIC) study [J].
Ballantyne, CM ;
Hoogeveen, RC ;
Bang, H ;
Coresh, P ;
Folsom, AR ;
Chambless, LE ;
Myerson, M ;
Wu, KK ;
Sharrett, AR ;
Boerwinkle, E .
ARCHIVES OF INTERNAL MEDICINE, 2005, 165 (21) :2479-2484
[3]   Lipoprotein-associated phospholipase A2, high-sensitivity C-reactive protein, and risk for incident coronary heart disease in middle-aged men and women in the Atherosclerosis Risk in Communities (ARIC) study [J].
Ballantyne, CM ;
Hoogeveen, RC ;
Bang, H ;
Coresh, J ;
Folsom, AR ;
Heiss, G ;
Sharrett, AR .
CIRCULATION, 2004, 109 (07) :837-842
[4]   A prospective evaluation of lipoprotein-associated phospholipase A2 levels and the risk of future cardiovascular events in women [J].
Blake, GJ ;
Dada, N ;
Fox, JC ;
Manson, JE ;
Ridker, PM .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2001, 38 (05) :1302-1306
[5]   Plasma PAF-acetylhydrolase in patients with coronary artery disease: results of a cross-sectional analysis [J].
Blankenberg, S ;
Stengel, D ;
Rupprecht, HJ ;
Bickel, C ;
Meyer, J ;
Cambien, F ;
Tiret, L ;
Ninio, E .
JOURNAL OF LIPID RESEARCH, 2003, 44 (07) :1381-1386
[6]   Enhanced association of platelet-activating factor acetylhydrolase with lipoprotein (a) in comparison with low density lipoprotein [J].
Blencowe, C ;
Hermetter, A ;
Kostner, GM ;
Deigner, HP .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (52) :31151-31157
[7]   Association of lipoprotein-associated phospholipase A2 levels with coronary artery disease risk factors, angiographic coronary artery disease, and major adverse events at follow-up [J].
Brilakis, ES ;
McConnell, JP ;
Lennon, RJ ;
Elesber, AA ;
Meyer, JG ;
Berger, PB .
EUROPEAN HEART JOURNAL, 2005, 26 (02) :137-144
[8]   Inhibition of lipoprotein-associated phospholipase A2 diminishes the death-inducing effects of oxidised LDL on human monocyte-macrophages [J].
Carpenter, KLH ;
Dennis, IF ;
Challis, IR ;
Osborn, DP ;
Macphee, CH ;
Leake, DS ;
Arends, MJ ;
Mitchinson, MJ .
FEBS LETTERS, 2001, 505 (03) :357-363
[9]   Lipoprotein-associated phospholipase A2, platelet-activating factor acetylhydrolase:: a potential new risk factor for coronary artery disease [J].
Caslake, MJ ;
Packard, CJ ;
Suckling, KE ;
Holmes, SD ;
Chamberlain, P ;
Macphee, CH .
ATHEROSCLEROSIS, 2000, 150 (02) :413-419
[10]   Relationship of molecular structure to the mechanism of lysophospholipid-induced smooth muscle cell proliferation [J].
Chai, YC ;
Binion, DG ;
Chisolm, GM .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2000, 279 (04) :H1830-H1838
123456